Abstract
BackgroundSomitogenesis is the earliest sign of segmentation in the developing vertebrate embryo. This process starts very early, soon after gastrulation has initiated and proceeds in an anterior-to-posterior direction during body axis elongation. It is widely accepted that somitogenesis is controlled by a molecular oscillator with the same periodicity as somite formation. This periodic mechanism is repeated a specific number of times until the embryo acquires a defined specie-specific final number of somites at the end of the process of axis elongation. This final number of somites varies widely between vertebrate species. How termination of the process of somitogenesis is determined is still unknown.ResultsHere we show that during development there is an imbalance between the speed of somite formation and growth of the presomitic mesoderm (PSM)/tail bud. This decrease in the PSM size of the chick embryo is not due to an acceleration of the speed of somite formation because it remains constant until the last stages of somitogenesis, when it slows down. When the chick embryo reaches its final number of somites at stage HH 24-25 there is still some remaining unsegmented PSM in which expression of components of the somitogenesis oscillator is no longer dynamic. Finally, we identify a change in expression of retinoic acid regulating factors in the tail bud at late stages of somitogenesis, such that in the chick embryo there is a pronounced onset of Raldh2 expression while in the mouse embryo the expression of the RA inhibitor Cyp26A1 is downregulated.ConclusionsOur results show that the chick somitogenesis oscillator is arrested before all paraxial mesoderm is segmented into somites. In addition, endogenous retinoic acid is probably also involved in the termination of the process of segmentation, and in tail growth in general.
Highlights
Somitogenesis is the earliest sign of segmentation in the developing vertebrate embryo
presomitic mesoderm (PSM) elongation is not happening at the same speed as somite formation To investigate the cessation of the process of somitogenesis in the chick tail bud it is important first to know if as previously proposed, the somites extend to the tip of the tail at Hamburger Hamilton (HH) stage 22 [30] or whether this is not the case and there remains some unsegmented PSM [26,28]
The somites extending close to the tip would indicate there is an imbalance between the speed of axis elongation and the recruitment of new cells to become part of the PSM tissue, while if the paraxial mesoderm remains unsegmented this would indicate that the somitogenesis oscillator stops producing somites at a specific stage of development
Summary
Somitogenesis is the earliest sign of segmentation in the developing vertebrate embryo This process starts very early, soon after gastrulation has initiated and proceeds in an anterior-to-posterior direction during body axis elongation. It is widely accepted that somitogenesis is controlled by a molecular oscillator with the same periodicity as somite formation This periodic mechanism is repeated a specific number of times until the embryo acquires a defined specie-specific final number of somites at the end of the process of axis elongation. During this process vertebrate embryos generate transitory structures called somites that later in development give rise to the vertebral column, most of the skeletal musculature and much of the dermis [4] At first considered to be a homogeneous blastema of tissue, lineage analysis has since shown that distinct stem cell populations exist in specific domains within the tail bud, as proposed by Pasteels [12], and they are capable of contributing to multiple tissue types [5,13,14,15,16,17,18,19,20]
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